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已发表论文
靶向乳酰化为逆转细胞死亡抗性提供治疗手段
Authors Wang Y , Chen J, Wang Y, Cao Y, Li Y, Zhu Y, Zhang Z, Wu S, Wang H
Received 14 September 2025
Accepted for publication 11 December 2025
Published 20 December 2025 Volume 2025:19 Pages 11371—11394
DOI https://doi.org/10.2147/DDDT.S567488
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Anastasios Lymperopoulos
Yumin Wang,1,* Jinxia Chen,2,* Yan Wang,3,* Yuwei Cao,1 Yulin Li,1 Yonglin Zhu,1 Zhe Zhang,1 Shuang Wu,4 Hongquan Wang5– 7
1Department of Respiratory and Critical Care Medicine, Aerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, 100049, People’s Republic of China; 2Department of Blood Transfusion, The Fourth Hospital of Hebei Medical University, Shijiazhuang, 050000, People’s Republic of China; 3Hunan Provincial Key Laboratory of Hepatobiliary Disease Research & Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital of Central South University, Changsha, 410011, People’s Republic of China; 4Department of Neurology, Zhongnan Hospital of Wuhan University, Wuhan, 430000, People’s Republic of China; 5Department of Geriatrics, Aerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, 100049, People’s Republic of China; 6Aerospace Medical Center, Aerospace Center Hospital, Beijing, 100049, People’s Republic of China; 7Inner Mongolia Key Laboratory of Allergic Diseases, Foundational and Translational Medical Research Center, Department of Allergy and General Surgery, Hohhot First Hospital, Hohhot, 010030, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Shuang Wu, Email wushuang0203@whu.edu.cn Hongquan Wang, Email whongquan@alu.fudan.edu.cn
Abstract: Lactylation, a lactate-derived post-translational modification, emerges as a master metabolic regulator of resistance to regulated cell death (RCD) across pathologies including cancer, inflammatory disorders, and degenerative diseases. By dynamically modifying histones and non-histone proteins via lactyltransferases and delactylases, lactylation orchestrates convergent molecular pathways that suppress ferroptosis, cuproptosis, and apoptosis. This review synthesizes current understanding of lactylation as a central regulator of RCD resistance in diseases, especially in cancers. We dissect the molecular machinery through which lactylation subverts ferroptosis, cuproptosis, and apoptosis; evaluate its pathophysiological implications in diverse pathologies; and discuss emerging therapeutic strategies to disrupt lactylation-mediated cell death evasion. This metabolic-epigenetic crosstalk establishes a robust shield against RCD in disease microenvironments, promoting therapeutic resistance and pathological resilience. Targeting lactylation regulators (writers/erasers) or combining lactate modulation with RCD inducers represents a promising strategy to overcome treatment-refractory conditions in cancers.
Keywords: lactylation, regulated cell death, ferroptosis, cuproptosis, apoptosis
1Department of Respiratory and Critical Care Medicine, Aerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, 100049, People’s Republic of China; 2Department of Blood Transfusion, The Fourth Hospital of Hebei Medical University, Shijiazhuang, 050000, People’s Republic of China; 3Hunan Provincial Key Laboratory of Hepatobiliary Disease Research & Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital of Central South University, Changsha, 410011, People’s Republic of China; 4Department of Neurology, Zhongnan Hospital of Wuhan University, Wuhan, 430000, People’s Republic of China; 5Department of Geriatrics, Aerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, 100049, People’s Republic of China; 6Aerospace Medical Center, Aerospace Center Hospital, Beijing, 100049, People’s Republic of China; 7Inner Mongolia Key Laboratory of Allergic Diseases, Foundational and Translational Medical Research Center, Department of Allergy and General Surgery, Hohhot First Hospital, Hohhot, 010030, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Shuang Wu, Email wushuang0203@whu.edu.cn Hongquan Wang, Email whongquan@alu.fudan.edu.cn
Abstract: Lactylation, a lactate-derived post-translational modification, emerges as a master metabolic regulator of resistance to regulated cell death (RCD) across pathologies including cancer, inflammatory disorders, and degenerative diseases. By dynamically modifying histones and non-histone proteins via lactyltransferases and delactylases, lactylation orchestrates convergent molecular pathways that suppress ferroptosis, cuproptosis, and apoptosis. This review synthesizes current understanding of lactylation as a central regulator of RCD resistance in diseases, especially in cancers. We dissect the molecular machinery through which lactylation subverts ferroptosis, cuproptosis, and apoptosis; evaluate its pathophysiological implications in diverse pathologies; and discuss emerging therapeutic strategies to disrupt lactylation-mediated cell death evasion. This metabolic-epigenetic crosstalk establishes a robust shield against RCD in disease microenvironments, promoting therapeutic resistance and pathological resilience. Targeting lactylation regulators (writers/erasers) or combining lactate modulation with RCD inducers represents a promising strategy to overcome treatment-refractory conditions in cancers.
Keywords: lactylation, regulated cell death, ferroptosis, cuproptosis, apoptosis